[Vårdfacket's language school. 2. Recruiting nursing students].
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Biomedical subjects
Publications and source records attributed to J Larsson.
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Forty-two patients (mean age 79 years) with acute ischaemia of one leg were evaluated in a prospective study. Forty-nine percent of the patients suffered from embolism, 29% from thrombosis while the etiology was uncertain in 22%. In 30 of the ischaemic legs and in 21 contralateral non-ischaemic legs the muscle energy metabolic status (ATP, ADP, AMP, ECP, PC, Cr and lactate) from the gastrocnemius muscle was measured and compared to values obtained from 24 healthy age-matched controls. There was a high degree of energy metabolic impairment in the ischaemic legs. Furthermore, the contralateral non-ischaemic legs were also energy depleted in comparison with those of the healthy controls. Legs with thrombosis were more energy-deprived than legs with embolism. Clinical evaluation of the degree of ischaemia and the level of occlusion correlated with energy metabolic parameters but the duration of ischaemia did not. The degree of metabolic impairment had no prognostic implication for the clinical outcome.
In traumatic injuries to the extremities, with a circulatory insufficiency, the resultant ischemia leads to decreasing levels of the energy-rich compounds adenosine triphosphate (ATP) and phosphocreatine (PCr) and increasing levels of lactate in muscle. A tourniquet model for temporary ischemia was used to determine if hyperbaric oxygen treatment could enhance the cellular metabolic restitution when the circulation was restored. The circulation of the rat hindlimb was interrupted for 1.5 and 3 hours. After 1.5 hours of ischemia, the levels of adenosine triphosphate, phosphocreatine, and lactate were restored to normal in muscle biopsies taken 5 hours after the ischemia. After 3 hours of ischemia, there were marked reductions of adenosine triphosphate and phosphocreatine and elevated lactate values in the postischemic muscle, indicating severe ischemic damage. Hyperbaric oxygen treatment at 2.5 atm for 45 minutes reduced these changes significantly. A certain number of hyperbaric oxygen treatments were necessary to maintain this effect. It is concluded that repeated hyperbaric oxygen treatments in the postischemic phase stimulate aerobic metabolism.
Owing to the high content of cyst(e)ine and sulphated mucopolysaccharides in skin tissues, an increased demand for sulphur amino acids could be expected during the anabolic phase in severely burned patients. As a marker for sulphur amino acid deficiency, leucocyte glutathione, methionine and taurine concentrations and urinary excretion of sulphur amino acids and inorganic sulphate were followed in five severely burned patients during a 5-month period (1-6 months post injury). Reduced leucocyte concentrations of glutathione, methionine and taurine, and decreased urinary excretion of inorganic sulphate, methionine, cyst(e)ine and taurine were observed, and were most pronounced 2 or 3 months after injury. Simultaneously a minor decrease in urinary output and leucocyte concentration of branched-chain amino acids and serine were also found, whereas normal levels of glycine, threonine, and glutamine were registered. The episode of limited availability of sulphur amino acids coincides with the period of most intensive collagen and keratin resynthesis of burned skin tissue.
Chronic idiopathic constipation requires surgical treatment in some rare cases. Seven such patients are presented. Subtotal colectomy was performed in six of them and left hemicolectomy in one. All patients were satisfied, with 1-6 bowel movements daily, and none had complications necessitating surgery. Subtotal colectomy seems to be the preferable operation.
The effect of a high energy missile trauma on energy metabolism and tissue oxygenation in uninjured parts of skeletal muscle was studied in anaesthetized pigs up to 72 hours after the trauma. High energy phosphates (HEP) were measured in muscle biopsies, and muscle tissue oxygenation was measured as muscle surface oxygen pressure fields by an oxygen electrode. In the traumatized group significantly decreased levels of HEP were found in spite of normal tissue oxygenation 72 hours after the trauma. In the control group both the HEP and the muscle tissue oxygenation were unchanged compared to the pretrauma situation. Decreased synthesis of HEP due to tissue hypoxia or inadequate nutrition could not account for the difference between the control and the trauma group. It was suggested that hypermetabolism induced by the high energy trauma caused increased utilization and thereby decreased concentrations of the HEP 72 hours after the trauma. It was also concluded that the general posttraumatic metabolic changes found in uninjured parts of the muscle tissue differed from the local changes of traumatized muscle described by other investigators, and therefore probably were caused by other mechanisms.
The changes in water and electrolyte metabolism associated with severe injury and sepsis are well recognized but changes in tissue content have seldom been available. This report combines the experience obtained from muscle biopsies of such patients performed in two centers; one located in Sweden and one in the U.S. Normal values for muscle water and electrolytes in each center are in close agreement. Needle biopsies of muscle were performed in 45 Swedish patients and 17 U.S. patients at intervals after injury or infection from the second to the thirtieth day. The patients' nutrition varied from brief periods of hypocaloric intake to prolonged high calorie parenteral nutrition with and without amino acids, as well as with and without fat. Prominent changes appeared during the first week and persisted up to 30 days regardless of the associated nutritional intake. These changes included an increased total muscle water, extracellular water, sodium and chloride and a decrease in muscle potassium and magnesium. This study demonstrates a simultaneous expansion of extracellular volume and a loss of intracellular components. This is in contrast to the experiences reported with less severe injury such as elective operation, where a more modest expansion of extracellular volume is seen and which is not associated with any loss of potassium or magnesium. The magnitude and persistence of these changes in muscle tissue deserve further study, both as to mechanism and implications for therapy.
To investigate hemodynamic and biochemical changes in acutely ischemic leg muscle, the arterial flow to one hind leg was reduced to 5% of resting flow in nine pigs. Blood sampled from the aortic arch and femoral vein before and during ischemia and during 2.5 hours of reperfusion was analyzed and blood flow was measured in the femoral artery. The flow increased to 140% of preischemic values after 10 min of reperfusion and thereafter normalized. Efflux of potassium, magnesium, CK, LDH and ASAT increased only slightly during ischemia, but responded immediately to reperfusion, with maxima at 2-10 min, and thereafter declined to around normal values. Venous pH in the leg fell in the first 2.5 hours of ischemia (7.32-7.11), then remained constant until reperfusion started, when a nadir of 6.99 was reached, and rose to 7.29 by the end of the study. O2 consumption in the leg increased 3.8 times from preischemia to 1 min after reperfusion. Control pigs did not show the mentioned changes. This standardized ischemic trauma resembles the situation in humans with severe unilateral leg ischemia and can facilitate investigations of response to medication.
In nine pigs the arterial blood flow to one hind leg was reduced to 5% of resting values during 8 hours in order to study changes in muscle energy metabolism. Biopsy samples from the gastrocnemius muscle were analyzed for ATP, ADP, AMP, PC, Cr, lactate, pyruvate, glycogen and pH before ischemia, at the end of the ischemic period and during 2.5 hours of reperfusion. During ischemia ATP/TCr decreased to 25%, ECP to 80% and PC/TCr to 6% of preischemic values. Lactate increased eightfold and glycogen fell to 40%. In the reperfusion period, lactate decreased to 1/3 of the end-ischemic value, PC/TCr showed threefold rise and ATP/Cr doubled. TCr fell to 66% of preischemic value. Other changes were not significantly affected by reperfusion. The end-ischemic values indicated severe ischemia, but some improvement of metabolism occurred during early reperfusion. The pig model is suitable for further studies aiming to improve the energy state of the cells during ischemia.
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